Abstract/Text: Two newly proposed infectious encephalitis/encephalopathy syndromes, in which magnetic resonance imaging (MRI) is essential for the diagnosis, have been reviewed. Acute encephalopathy with biphasic seizures and late reduced diffusion (AESD) is reported only in East Asian infants, characterized by a febrile seizure (usually >30 min) as the initial neurological symptom on day 1, followed by secondary seizures at day 4 to 6; affected children display variable levels of neurological sequelae. MRI shows no acute abnormality during the first two days; reduced diffusion appears in the frontal or fronto-parietal subcortical white matter during days 3 to 9, then disappears between days 9 and 25. Excitotoxic injury with delayed neuronal death is hypothesized as a possible mechanism based on MR spectroscopic findings. Clinically mild encephalitis/encephalopathy with a reversible splenial lesion (MERS) is characterized by a reversible lesion with homogeneously reduced diffusion in the corpus callosum (at least involving the splenium), sometimes associated with symmetrical white matter lesions. The most common neurological symptom is delirious behavior, followed by consciousness disturbance, and seizures, all of which completely recover within a month. The reason for the transiently reduced diffusion within the lesions is unknown; possibilities that have been postulated include intramyelinic edema, interstitial edema in tightly packed fibers, and a transient inflammatory infiltrate.

Abstract/Text: Two newly proposed infectious encephalitis/encephalopathy syndromes, in which magnetic resonance imaging (MRI) is essential for the diagnosis, have been reviewed. Acute encephalopathy with biphasic seizures and late reduced diffusion (AESD) is reported only in East Asian infants, characterized by a febrile seizure (usually >30 min) as the initial neurological symptom on day 1, followed by secondary seizures at day 4 to 6; affected children display variable levels of neurological sequelae. MRI shows no acute abnormality during the first two days; reduced diffusion appears in the frontal or fronto-parietal subcortical white matter during days 3 to 9, then disappears between days 9 and 25. Excitotoxic injury with delayed neuronal death is hypothesized as a possible mechanism based on MR spectroscopic findings. Clinically mild encephalitis/encephalopathy with a reversible splenial lesion (MERS) is characterized by a reversible lesion with homogeneously reduced diffusion in the corpus callosum (at least involving the splenium), sometimes associated with symmetrical white matter lesions. The most common neurological symptom is delirious behavior, followed by consciousness disturbance, and seizures, all of which completely recover within a month. The reason for the transiently reduced diffusion within the lesions is unknown; possibilities that have been postulated include intramyelinic edema, interstitial edema in tightly packed fibers, and a transient inflammatory infiltrate.

Abstract/Text: BACKGROUND: Every year, an estimated 200-500 children in Japan develop influenza-associated encephalopathy (IAE), and 10-30% of these children die.
OBJECTIVE: To clarify the clinical features of a severe form of acute encephalopathy seen with 2009 pandemic influenza A (H1N1).
STUDY DESIGN: This retrospective survey examined 20 children with acute encephalopathy associated with the 2009 pandemic influenza A (H1N1) who died or were in a prolonged deep coma with a flat electroencephalogram tracing and loss of spontaneous respiration. We obtained demographic, clinical, laboratory, and neuroimaging data through interviews with the attending physicians and chart reviews.
RESULTS: Subjects were 13 boys and seven girls. Their median age was 45 (range 11-200) months. Five patients had one or more pre-existing conditions. Acute encephalopathy developed within 2 days after influenza onset in 16 patients. As the initial neurological symptom, delirious behavior was seen in six children, and brief seizures in six. Eighteen patients were comatose within 6h of the onset of encephalopathy. Marked brain edema on computed tomography (CT) was seen in all but one patient. Brainstem lesions on CT were recognized in 12 patients. Sixteen patients died 0-45 (median 2.5) days after the onset of acute encephalopathy, and the others remained in deep comas without spontaneous respiration.
CONCLUSIONS: The clinical course of the patients was characterized by an onset with mild neurological symptoms and rapid deterioration of consciousness into coma. Head CT revealed marked cerebral edema, often associated with brainstem lesions.

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